H. Edward Durham Jr., CVT, LATG
One of the defining characteristics of mammals is the four chamber quadra-valved heart. Blood flow in mammals proceeds from the left ventricle through the body's systemic capillary beds returning to the right atrium, on to the right ventricle and out to the lungs to obtain more oxygen and release carbon dioxide, returning to the left ventricle via the pulmonary veins and left atrium. The mammalian heart also contains an electrochemical conduction system that stimulates the myocardium to contract causing blood to flow. The basic physiologic and pathophysiologic principles are broadly similar between mammalian species, yet breed and species differences do exist. This presentation seeks to review equine cardiology and the cardiac conditions common to horses.
Exercise physiology is an important component of equine cardiology as so much of human interaction with horses is a result of athletic pursuits. Assessing the athletic ability of horses is an area of ongoing research. Many cardiovascular indices have been evaluated or are being actively investigated, but no single parameter has been found that will accurately predict a horse's future performance.
Perhaps one of the simplest indices is the evaluation of heart rate (HR). It is well accepted that the better an athlete's conditioning the lower their HR at a given level of exercise. In fact the relationship of HR to work effort is linear at sub-maximal exercise. This observation is true for equine athletes as well. At rest the healthy horse has a HR of 24-48 bpm, but at peak exercise the HR may reach 240-260 bpm. Perhaps one of the most common methods of evaluating performance based on HR is V140 and V200 or the horse's velocity at a HR of 140 or 200. Simply stated, this test asks the question, how fast is the horse running when its HR reaches 140 or 200 bpm? By running a horse on a treadmill and attaching an ambulatory electrocardiograph (ECG) monitor, one can record the velocity of the treadmill when the HR reaches the target. A better performer should have a higher V140 or V200.
Another method of assessing cardiovascular performance is to look at the maximal uptake of oxygen (O2) possible for an individual athlete. This index is called VO2 max and also has a linear relationship with HR, which makes the use of HR monitoring useful since it is so closely linked with O2 demand. When prolonged sub maximal work is undertaken the HR tends to plateau and stabilize until a higher level of work is performed, although some cardiac drift may occur, especially in dehydrated animals (as seen with prolonged exercise).
Post exercise HR has also been used to evaluate fitness. Following exercise the HR falls quite quickly to a steady-state higher than the resting HR for a short period then gradually decreases to normal. Horses with a higher post exercise heart rate tend not to perform as well as those with lower post exercise HR. Research demonstrated that endurance horses that had a resting HR of greater than 65-70 after 30 minutes were much more likely to not finish or to finish poorly and horses with a HR 60 bpm after 30 minutes (HR >50 bpm not uncommon post exercise) had less evidence of dehydration during a rest period echocardiogram.1 Rapid HR recovery (post exercise) implies better cardiovascular health. Interestingly, stroke volume reaches its maximum at 40% of VO2 max and further increases of cardiac output result from increases in HR. Cardiac output, or the volume of blood pumped by the heart in one minute increases from about 20 at rest to nearly 300 liters during peak exercise.
Several studies have investigated the use of ECG changes to predict performance. The Heart Score is the mean of the QRS durations (ms) in the bipolar leads and was shown to be correlated with Thoroughbred earnings in one study.2 Additional research has not supported those findings. Another method evaluated changes in T wave morphology as a sign of myocarditis in horses with poor race performance. Again further research has brought doubt on T wave morphology as a clinical tool. At this time, the ECG is not thought to give much information on performance other than ruling out clinical arrhythmias that might reduce performance. Echocardiographic indices of heart size have been related to performance in which better performing horses also showed slightly larger cardiac size by echocardiography in some but not all studies. However, the predictive value may be limited and be best suited for equine endurance athletes.3
Histories of exercise intolerance, poor performance, identification of arrhythmias and/or murmurs are the most common justifications for presentation to the cardiology service. Some horses present with ventral subcutaneous edema, fever of unknown origin or rarely, coughing. Many murmurs are detected during routine veterinary care or pre-purchase examinations. When a significant cardiac condition suspected a complete physical examination should be performed, with attention to those aspects of the examination specific to the cardiovascular system. Before exciting the patient with palpations, the examiner should observe the horse's respiratory effort and rate. One should observe the patient's jugular veins for distension or pulsation. Pulsations that extend higher than the lower third of the neck are abnormal, implying elevated right atrial pressure and tricuspid regurgitation (TR). Care must be given in this assessment not to confuse carotid pulses under the jugular vein as jugular pulsations. This false positive finding is especially common in thin horses. Arterial pulses can be felt in the facial artery under the proximal third of the jawbone. Hypokinetic pulses are associated with conditions that cause hypotension. Hyperkinetic pulses can be detected with significant aortic regurgitation (AR). This area can also be used to palpate pulses during auscultation to evaluate for pulse deficits. One should also palpate the left hemithorax for the presence of palpable vibrations or "thrills" associated with murmurs and the apical impulse. Auscultation typically begins over the mitral valve area, about which is located about the 5th-6th intercostal space just caudal to the left elbow, and proceeds cranially and dorsally where the semilunar valves are evaluated. The S1 sound and murmurs of mitral regurgitation MR are best heard in this area. Note the HR and rhythm for arrhythmias. Foals have higher HR than adults; around 80-120 bpm that gradually slows as they age. Before auscultating the right hemithorax should be palpated for thrills.
During cardiac auscultation it is normal to hear the four sounds of the cardiac cycle; the first and second heart sounds (lub & dub) typically heard in all mammals and two additional sounds (S3 and S4) associated with ventricular filling are usually appreciated in horses. The S4 sound also called the "atrial contraction sound" and denotes atrial systole.
A number of murmurs may be detected in horses. The two most common murmurs are functional murmurs and (MR) due to valvular degeneration. Functional murmurs are usually systolic murmurs which occur in a structurally normal heart and are very common in horses. One study reported functional murmurs occurring in 66% of horses1. Another common cause of systolic murmurs, especially in young horses, is ventricular septal defect (VSD). This murmur generally radiates toward the right sternum and can be quite loud. Diastolic murmurs of AR, which have been described as a "dive bomber" sound, are also heard in the clinically normal animal and are not uncommon. One can sometimes hear a systolic/diastolic combination murmur or "to/fro" murmur. This unusual murmur can be heard in healthy animals with functional murmurs or in aged horses with valvular degeneration. It is distinguished from the continuous murmur by a short break in the sound that occurs when the heart changes from systole to diastole. Continuous murmurs of patent ductus arteriosus can be heard during examination of young foals less than a week old but are extremely rare in adult horses. Also, pre-systolic (S4) and S3 filling murmurs may also be heard in clinically normal animals.
One important clinical challenge is to distinguish functional murmurs from MR. They can partly be differentiated by their timing. The murmur of MR is typically holosystolic (lasting throughout the duration of systole), whereas functional murmurs tend to be restricted to early systolic to mid-systolic periods. With regard to location, functional murmurs are best heard over the heart base and MR murmurs best over the left apical impulse. Functional murmurs tend to change with exercise. After exercise the murmur may increase or decrease in intensity. Functional murmurs typically have a crescendo or decrescendo pitch in contrast to the MR sound of a plateau shaped murmur that changes little in intensity. Echocardiography is the best diagnostic tool to identify the cause of a murmur.
A summary of major equine murmurs by their timing reveals the systolic murmurs to include: functional murmur, MR, TR, and the VSD. The murmurs of diastole include: presystolic (S4), S3 filling, and AR. There is always the potential for a to/fro murmur as well. Diseases of the pericardium can produce rubbing, or knocking sounds, with pericardial disease. These sounds can occur at any time during the cardiac cycle when the heart is in motion.
Electrocardiography is a valuable tool for assessing equine cardiac rate and rhythm. Due to the conduction system of the horse, an ECG's usefulness is limited in other cardiac assessments. Horses have a different cardiac conduction system compared with dogs. In the dog, the Purkinje fibers extend along the endocardium and the impulse is carried to the rest of the heart via cell to cell depolarization. In horses, the conduction fibers extend to the epicardium and endocardium allowing for nearly simultaneous depolarization of the entire myocardium at once. Consequently, unlike in dogs, the mean electrical axis cannot be calculated to detect cardiac chamber enlargement. Although possible, it becomes unnecessary to perform a recording in the frontal plane to create the hexaxial lead system. The standard method of recording the ECG in horses is from the base-apex lead, or a negative electrode at the right jugular furrow (typically white) and a positive electrode (black or red) at the left precordial apical impulse with a ground electrode attached in an unobtrusive place. A typical equine ECG recorded in the fashion demonstrates a positive "P" wave, negative "QRS" complex and positive "T" wave for which normal values are published.1
Echocardiography can be used for assessment of cardiac chamber size and systolic function. By imaging from both sides of the horse, the entire heart can usually be visualized except in some large draught horses. Precise measurements can be taken and murmurs can be located using color flow Doppler. The experienced echo-sonographer can calculate pressure differences based on the velocity of blood movement through the heart. Cardiac masses and pericardial effusion can be identified. An echocardiogram can be useful for horses with AF about to undergo quinidine therapy to assess the overall heart function before it is suppressed by therapy.
Arrhythmia detection and characterization represent an important part of the examination as arrhythmias are commonly associated with poor performance. Fortunately, most arrhythmias detected in horses are physiological and manifest no clinical signs. Perhaps the most common arrhythmia is 2nd degree atrioventricular block. This physiologic arrhythmia is related to strong vagal tone seen in horses and abates with exercise. Impulses from the sinus node are blocked at the atrioventricular node when the horse is calm and sympathetic tone is low. When stimulated and sympathetic tone increases, it overrides the parasympathetic vagal tone and the block disappears. Other arrhythmias of no clinical significance are transient sinus arrhythmia that may be seen following exercise, sinoatrial block, wandering pacemaker, and 1st degree atrioventricular block. Equine patients presenting with gastrointestinal disease may show premature atrial complexes on an ECG arrhythmias that can be detected during auscultation.
Atrial fibrillation (AF) is an abnormal cardiac rhythm that can occur in equines and bovines with normal hearts, and is of clinical importance in horses, as it is a leading cause of non-lameness performance reduction. Atrial fibrillation may sometimes occur transiently during or after exercise. If AF is sustained it can decrease cardiac performance leading to a reduction in cardiac output and therefore overall performance. Atrial fibrillation in horses is characterized by an undulating baseline with no clear "P" waves. Although the rhythm is irregular, the rate is typically within normal limits due to the equine vagal system. The "QRS" complexes have a normal morphology.
Since AF in many horses occurs in ostensibly normal myocardial tissue, treatments that convert the arrhythmia to sinus rhythm are preferred. Before treatment begins a standard base-apex ECG should be obtained. The "QRS" complex duration should be measured and recorded before initiating therapy. If the "QRS" duration increases by more than 25% during treatment, quinidine therapy should be discontinued. In most cases, AF is treated with oral quinidine sulphate administered via nasogastric tube. Treatment of AF with quinidine is not without its challenges. Quinidine has a narrow limited therapeutic range of only 2-5 µg/ml with several side effects including hypotension, tachycardias, alterations of conduction, CHF, sudden death, colic, diarrhea, ataxia, laminitis, airway obstruction, urticaria and/or wheals and depression. Close observation is an essential part of quinidine therapy. Continuous ECG monitoring is ideal to watch for prolongation of the "QRS" complex, ventricular arrhythmias or supraventricular tachycardias.
Quinidine is usually administered every 2 hours for the first four doses and then blood levels are checked. Dosing is reduced to approximately every 6 hours until conversion occurs. Blood quinidine levels should be checked as needed. If after two days the AF persists, additional treatment with digoxin can be implemented. This protocol requires extreme care since quinidine and digoxin compete for the same receptor site and can predispose the patient to digoxin toxicity. Toxic side effects of digoxin overlap those of quinidine a great deal so the assault to the gastrointestinal system and the cardiovascular system is especially severe. Care must be taken when converting horses with AF to sinus rhythm. Close monitoring and prompt treatment of side effects is essential. It is important to remember that AF also occurs with heart disease and these horses are much less likely to convert back to sinus rhythm.
Recently, new antiarrhythmics such as flecainide and amiodarone have been evaluated for converting AF to a sinoatrial rhythm. Research is ongoing, with amiodarone holding promise; however flecainide may be limited to use in acute AF. Perhaps the boldest therapy is transvenous electrical cardioversion. During this cardiac catheterization procedure, special electrode-tipped catheters are advanced into the right heart and an electrical current applied to defibrillate the atrial tissue returning the patient to sinus rhythm. This therapy requires special equipment and general anesthesia.
Ventricular arrhythmias and 3rd degree or complete AVB are also seen in horses. Ventricular arrhythmias can be treated with lidocaine or in the case of refractory ventricular tachycardia, magnesium sulphate. Horses with complete AVB must, like humans or dogs, receive a permanent pacemaker.
Congenital Heart Disease
Ventricular septal defects (VSD) are the most commonly reported congenital defect in horses. These developmental defects can range from life threateningly severe to incidental. Murmurs of VSD are typically grade 3 or higher systolic right sided murmurs that radiates toward the sternum. Many VSDs are small and restrictive, meaning the diameter is small enough that most flow through the defect is inconsequential. It is not uncommon to find a restrictive VSD as an incidental finding during echocardiogram in an otherwise normal horse. These defects are in the membranous region of the septum just under the aortic valve. If the defect is large, the added volume can over circulate the lungs and the left heart and can ultimately lead to left sided congestive heart failure (CHF). Alternatively, the aortic valve apparatus may be deformed and serious AR may result also leading to CHF. A less common VSD can be seen in the infundibular region near the pulmonic valve. This defect is interesting in that the resulting murmur sounds like pulmonic stenosis (PS) however since PS and aortic stenosis are quite rare in horses (unless they are seen as part of a more complex set congenital defects) it can be easily misdiagnosed by auscultation alone. Even with echocardiography the infundibular VSD can be difficult to diagnose. Complex congenital defects are most often seen in foals and are usually life threatening. Echocardiography is extremely helpful in evaluating congenital cardiac disease.
Acquired Heart Disease
As horses age they may develop a chronic myxomatous valvular degeneration that primarily affects the aortic and mitral valves. This degeneration can lead to valve incompetency, murmurs and, if regurgitation is severe enough, CHF. Mitral regurgitation from valvular degeneration is one of the most common causes of murmurs in horses. It is also a common cause of heart failure and can lead to pulmonary rupture and sudden death. Echocardiograms reveal thick valve leaflets that may prolapse into the left atrium. Color flow Doppler demonstrates large color jets crossing into the left atrium during systole creating a systolic murmur. Degeneration that affects the aortic valve may cause a diastolic murmur. As the aortic valve degenerates and more leakage occurs, the volume overload from blood moving back from the aorta eventually causes the ventricle to fail.
Fortunately for horses unlike dogs, cats, and humans, myocardial diseases in horses are uncommon. Dilated cardiomyopathy is virtually the only cardiomyopathy seen in horses and has been associated with heart failure. Echocardiographically it has the same hallmarks as seen in dogs or humans; a dilated left ventricle with poor contractility. The prognosis is poor for this condition.
Inflammatory conditions such as endocarditis and pericarditis are also seen in horses and can both present with a fever. The diagnosis of both of these conditions is aided by echocardiography. Pericardial effusion can be seen readily by ultrasound which can then be used to guide placement of cannula for fluid removal. Vegetative lesions on the valve due to endocarditis may be apparent by echocardiography, thereby supporting the clinical diagnosis and helping to assess the damage.
Lastly, toxicities such as ionophore toxicity and White snakeroot poisoning can lead to sudden death in horses from ventricular arrhythmias. Ionophore toxicity is typically introduced from cross contamination of cattle feed into the equine food source. Horses affected with ionophore toxicity need care for several months after exposure as the full effects can be delayed. White snakeroot toxicity (Eupatorium rugosum) can occur in any grazing stock in the Midwest, and can also lead to heart failure in horses.
Treatment of heart failure in horses is typically limited to the use of furosemide, digoxin and angiotensin converting enzyme inhibitors. These drugs can be used to relieve the symptoms of CHF but they can be expensive to use. Fortunately for horse lovers everywhere there are limited cardiac diseases in horses.
1. Marr C. 1999 Cardiology of the Horse, Saunders
2. Steele. Austrail Medical Pub 1963
3. Young LE, Wood JLN. ACVIM Proceed 2003